In FY 2019, we investigated how HPV integration could result in de novo super-enhancer formation in cervical cancer. We characterized the chromatin and genomic landscape of a super-enhancer associated HPV integration site using whole genome sequencing, RNAseq, ChIPseq and molecular combing/fiber-FISH. Targeted disruption of factors binding to this element decreases viral transcription and causes cell death. Thus, cancer cells harboring integrated HPV may be targeted by therapeutics that disrupt super-enhancer function.